The present invention is directed to an apparatus for providing hemostasis of dental pulp. In particular, the present invention is directed to an electrosurgical coagulation tool which provides durable hemostasis to exposed dental pulp with little or no damage to the pulp.
Teeth, both primary and permanent, consist of outer enamel, an inner layer of dentin, and a soft tissue component referred to as the dental pulp. The pulp is enclosed by dentin, is continuous with soft tissue in the tooth socket, begins at the tip of the root, traverses through each root and terminates in the pulp chamber of the coronal or visible portion of the tooth. Initially, the dental pulp is responsible for the development of the enamel and dentin and later continues to provide the blood supply, nerve enervation and lymphatic drainage. The pulp responds to insult by depositing reparative and secondary dentin to protect the pulp and initiates an inflammatory process to combat bacterial infection.
The tooth and pulp are typically threatened in a variety of ways: (1) fracture of the tooth exposing the pulp to bacteria normally present in the oral cavity; (2) dental caries (decay) which decalcifies enamel and dentin, exposes the pulp and allows ingress of bacteria and bacterial products, (3) dental restorative procedures which may inadvertently expose the pulp; and (4) failure of dental restorations through fracture or leakage, including microleakage, allowing bacteria or bacterial by-products to reach the pulp. For decades many factors have been blamed for causing inflammation and necrosis (i.e., non-vitality, death) of the dental pulp, including: (1) dental caries and associated bacteria being the most prominent; (2) fracture and exposure to bacteria; (3) excess heat from dental instrumentation; and (4) toxicity of dental materials. More recently, bacterial invasion via microleakage has been attributed as an important cause of pulpal inflammation and necrosis.
Traditionally, when a small exposure of the pulp occurred mechanically, by fracture of the tooth, or while excavating caries, the exposure was promptly xe2x80x98cappedxe2x80x99 with various dental materials in an attempt to prevent inflammation or necrosis of the pulp. If the exposure was small and capping occurred immediately and with a suitable material, pulpal necrosis could be averted. However, if the exposure was moderate or large in size, or if capping occurred after bacteria developed a foothold, or if the capping material deteriorated leading to microleakage, then inflammation or necrosis would typically occur. Materials (e.g., calcium hydroxide) which stimulated reparative dentin formation were used for capping of the pulp for over half a century in an attempt to stimulate health and to restore the pulpal wall naturally via slow deposition of reparative dentin.
If the pulp progressed to necrosis, only two options were available to the patient: (1) extraction of the tooth; or (2) extirpation of the necrotic pulp and filling of the pulpal space with a suitable material to prevent microleakage via the pulp space to the surrounding bone. This second alternative is referred to as endodontic therapy (root canal treatment). Inflamed vital dental pulps, however, represent a substantial portion of infected pulps. Additionally, pulps exposed intentionally for therapeutic purposes (e.g., to support a denture) also constitute a significant portion. These latter two groups are currently relegated to extraction or endodontic therapy despite their vitality. Inflamed but vital pulps are considered, under current clinical guidelines, to be untreatable. Even teeth with relatively mild symptoms are diagnosed as xe2x80x9cirreversible pulpitisxe2x80x9d and condemned to extraction or endodontic therapy.
Over the past seven decades, the research primarily centered around the stimulation of reparative dentin deposition and pulp therapy was limited to small exposures on asymptomatic teeth. A few reported exceptions involved more aggressive pulp therapy but was limited to adolescent and young adult patients. Several developments in the field opened the possibility of more comprehensive pulp therapy. These included: (1) The realization that most pulpal inflammation is due to bacteria invasion and bacterial by-products occurring via microleakage and less due to toxicity of dental materials; and (2) The development of materials that adhere to dentin and which can produce a seal to prevent microleakage (i.e., dentin adhesion products and the ability to create a hybrid layer consisting of collagen and resin). The ability to stimulate the deposition of reparative dentin became a standard for demonstrating re-organization and healing of the pulp after an insult. Despite these developments, only teeth with small exposures or mild clinical symptoms were routinely treated while the great majority of teeth exhibiting pulpal inflammation or periapical inflammation (inflammation of a pulpal origin in the bone around the tip of the root) were treated with endodontic therapy or extraction of the tooth.
One of the obstacles in treating the pulp is the impact of bleeding on the formation of the pulp barrier (sealing of the pulp or the restoration of the missing pulpal wall). Bleeding during any surgical procedure can impact on the success of treatment ranging from (1) being a mere nuisance or compromising visibility to (2) creating a toxic reaction (as in neurosurgery). Bleeding around the retina during eye surgery, for example, is an important concern. In pulp therapy, bleeding compromises visibility, jeopardizes the dentin adhesion and creates voids or tracts within the barrier material resulting in chronic irritation and failure of the pulp therapy. In a very common situation, pulp therapy cannot be instituted because the hemorrhaging cannot be controlled. In these cases, the teeth are relegated to endodontic therapy or extraction simply due to the uncontrolled bleeding. One might wonder why bleeding cannot be controlled in an exposure approximately 2-4 square mm in area and consisting of very small blood vessels when bleeding is routinely controlled in major surgical procedures where much larger vessels are involved. A good analogy can be made with ophthalmic surgery where even minor amounts of bleeding during the procedure can compromise the overall therapeutic effort. In pulp therapy, minor bleeding contaminates the surface of the dentin preventing adhesion of the pulp barrier and jeopardizing the valuable dentinal seal. Residual blood clots have been reported to prevent healing and even stimulate an inflammatory response by the release of chemotactic components.
Another important dilemma is that the bleeding must be controlled with little or no injury to the remaining pulp tissue. Furthermore, hemostatic procedures and materials which do not impact on the highly technique-sensitive dentinal adhesion process must be selected. These two factors place severe restrictions on the ability to control bleeding. Furthermore, temporary hemostasis is not sufficient since numerous procedures are required to create the pulp barrier and final restorationxe2x80x94any of which can cause recurring bleeding at a critical moment. Therefore, durable hemostasis is required with minimal or no injury (especially lasting injury) to the pulp. The present invention provides an apparatus which satisfies the need in the art for durable hemostasis.
Most efforts in controlling bleeding of the pulp involved application of a cotton pellet and light pressure until hemorrhaging ceased. This proved fairly effective with very small exposures but was ineffective with larger exposures or hyperemic pulps. Over the past century, pulpotomy procedures were quite common upon exposure of the pulp. Pulpotomy procedures typically remove the chamber portion of the pulp (the part of the pulp enclosed by the clinical crown, the visible portion of the tooth, as opposed to the pulp tissue contained within the root portion). This allowed control of bleeding at the more constricted portion of the pulp which was easier to accomplish. However, it meant sacrificing a substantial segment of vital pulp tissue. This approach is still quite common in children""s primary teeth.
Numerous vasoconstricting (blood vessel contracting) medicaments and even necrotizing materials have been used partly for hemorrhage control and partly for therapeutic purposes. More recently, with greater attention to gentle treatment of the pulp, the selection of materials or medicaments were directed at hemorrhage control with minimal effect on the pulp tissue and with minimal impact on the dentin adhesion procedures. Sodium hypochlorite (2-5%) has been advocated for use in this manner. The present state of the art in pulpal hemostasis consists of: (1) cotton pelletxe2x80x94dry, moist with water, or moist with saline; (2) Sodium hypochlorite (2-5%) applied and rinsed; or (3) failing to achieve hemostasisxe2x80x94referral for endodontics or extraction.
Monopolar electrosurgery uses an active electrode which is very small in dimension compared to the grounding electrode (referred to as the dispersive electrode). The applied power concentrates the current at the narrow point or blade of the active electrode. When sufficiently high, the current is released to the less conductive tissue via direct contact or as a spark that jumps to the tissue. The intense heat that is generated by this sequence of events, which occurs thousands of times per second, coagulates the tissue next to the active electrode. With the monopolar mode, the current then dissipates through the body of the patient via a path of least resistance to the dispersive electrode. Serious consequences have been reported associated to this dispersive path. In particular, there is the potential for necrosis of the pulp, never before realized in dentistry and identified by the inventor, due to a channeling effect of the dissipating current passing through a constriction of the tissue. Monopolar electrosurgery has been used in pulp therapy to fulgurate the pulp. Fulguration is the destruction or ablation of tissue caused by delivering a high frequency electrosurgical current. An electrode is applied a short distance from the tissue and a series of high intensity sparks are caused to jump from the electrode to the tissue causing ablation of the tissue. Fulguration was used much like formocresol, silver nitrate and other materials to coagulate, necrotize, cauterize, etc., a layer of tissue or the entire pulp. Fulguration also provided hemostasis although it is not clear whether it was ever used solely for hemostasis. Fulguration was shown to adversely affect the pulp and tissue surrounding the tooth. The hazards of using monopolar electrosurgery on the dental pulp or near metallic restorations in the tooth, has been reported in a number of publications. These hazards are related to the monopolar mode of electrosurgery, and accordingly, monopolar electrosurgery is contraindicated for use on or near the dental pulp.
The apparatus concerns an electrosurgical tool for use with a bipolar electrosurgical power unit for coagulating a tissue layer, for example, exposed pulp of a tooth. The tool has an elongated hand piece with a butt end and a head oppositely disposed. An electrical coupling is mounted on the butt end and adapted to connect electrically to the electrosurgical power unit. An electrically conductive pathway is arranged lengthwise along the hand piece and is connected to the electrical coupling. An elongated electrode is mounted on the head and connected to the electrically conductive pathway, the electrode being rotatable about its long axis and oriented at an angle relatively to the hand piece.
Preferably, the electrode is a coaxial bipolar electrode having a first electrode pole coaxially surrounded by a second electrode pole, an insulating layer being coaxially positioned between the first and the second poles. The electrode has an end face positioned distally to the head and asymmetrically arranged with respect to the long axis of the electrode. In one embodiment, the end face is formed by extending the first electrode pole lengthwise beyond the second electrode pole, the end face being oriented at an angle, asymmetrically relatively to the long axis by curving the electrode. In another embodiment, the end face is a cut-back region at the tip of the electrode formed by removing a lengthwise portion of the second pole and the insulating layer along one side of the electrode to expose the first pole along a portion of the one side.
Preferably, the head has a socket sized to receive the electrode for mounting it on the head, the socket having electrical contacts positioned therein, connecting the electrode to the electrically conductive pathway. The socket has a diameter smaller than the electrode to provide an interference fit to frictionally retain the electrode and allow it to rotate about its long axis but also retain its set position against light contact of the end face with a surface.